Liver fibrosis is characterized by the deposition of collagen and other extracellular matrix proteins and their organization in complex polymers, which are insoluble and induce loss of the liver architecture. Collagen and matrix proteins that constitute fibrosis are largely produced by activated hepatic stellate cells. The stellate cells are activated from a quiescent lipocyte phenotype to a fibroblastic phenotype. The activation occurs in two phases: initially, activation of stellate cells by cytokines (especially TGF-beta), chemokines and other signaling molecules induced by the inflammatory process, followed by transformation of the stellate cells into a myofibroblastic phenotype, in which the cell can proliferate, attract leukocytes and produce extracellular collagen and matrix proteins. In all forms of chronic hepatitis, active fibrosis begins around the portal areas (periportal zone or zone 1 fibrosis, Metavir fibrosis stage 1) and gradually extends out into the lobules towards the central veins (zone 3), with septa formation (Metavir fibrosis stage 2). Then, bridging occurs (Metavir fibrosis stage 3). The final stage of fibrosis (Metavir fibrosis stage 4) is early cirrhosis: extensive fibrosis linking portal and central areas, accompanied with nodular regeneration of the liver parenchyma. Other histological scores, apart from the Metavir system, are also often used, such as the HAI score. The HAI score distinguishes no fibrosis (grade 0) from mild, non-bridging fibrosis (grade 1); bridging fibrosis (grade 3) and early cirrhosis (grade 4). Liver fibrosis accompanies most chronic liver disorders and is characterized by the growth of scar tissue between areas of functional liver tissue. As such, growth of connective tissue is a normal reaction to tissue injury, but it can “overshoot,” resulting in liver fibrosis. The rate of progression of fibrosis is the disease-defining hallmark of chronic hepatic diseases, as it is this fibrosis progression that ultimately leads to architectural distortion of the liver, and to cirrhosis. It is important to assess the stage of fibrosis and the rate of progression of fibrosis, as some chronic liver disease patients progress rapidly, finally ending up with cirrhosis and the associated life-threatening complications, whereas others progress very slowly, if at all, and might never suffer from liver-associated complications. Therefore, liver biopsy is generally performed in newly diagnosed chronic liver patients. However, this is an invasive, often painful diagnostic technique that sometimes is accompanied with serious complications. Moreover, although it is considered to be the “gold standard” for fibrosis staging, liver biopsy might under-sample the true state of the liver disease, as only a small area is probed. Thus liver biopsy is not well suited as a routine follow-up tool. An ideal tool for the follow-up of liver fibrosis would be a non-invasive clinical bio-marker, the measured values of which should correlate with the fibrosis stage (the gradation of liver fibrosis). Several markers and marker sets have been evaluated towards this goal, but none of them fully satisfies these requirements. For example, extracellular matrix components present in serum have been used, with serum hyaluronic acid apparently being the most reliable one. Still, the consensus that seems to arise from the accumulating studies that involve this marker, is that it can be quite reliable to exclude cirrhosis in a number of patients (high negative predictive value), although its accuracy in cirrhosis detection is low (about 30% sensitivity). Binary logistic regression models such as “Fibrotest”, based on a range of clinical chemistry analytes have recently been much studied for these purposes (ref. 14, 15 and PCT International Patent Publication WO 0216949, the contents of the entirety of which is incorporated herein by this reference). However, these markers have a low sensitivity at the >95% specificity levels that would be required to obviate the need for biopsy in chronic liver disease patients, or to reliably detect the onset of early cirrhosis in a follow-up setting. It is clear that additional serum markers with high specificity and good sensitivity are needed for non-invasive monitoring of liver fibrosis and its progression. In the present invention, we have developed a “clinical glycomics” method that uses a standard PCR thermocycler and an automated DNA sequencer/fragment analyzer to rapidly generate high-resolution profiles of the N-glycan post-translational modifications present on the proteins in patient's serum. We show that the serum N-glycome yields a biomarker that distinguishes early cirrhotic from fibrotic liver disease patients with 79% sensitivity and 86% specificity. Importantly, when our new biomarker is used together with the clinical chemistry-based {Fibrotest} biomarker (which detects early cirrhosis in our invention with 92% sensitivity and 76% specificity), the specificity for the differentiation between fibrosis and early cirrhosis cases improved to 100%, while retaining a sensitivity of 75%.